Nematodes

Year III
Nematodes – General Characters
• Non-segmented cylindrical worms tapering at both ends
• Possess cuticle
• Sexes are separate (diecious), male is smaller than female and its
posterior end is curved ventrally
• Females are either
• Viviparous (produce larvae/ embryos)
• Oviparous (lay eggs) or
• Ovo-viviparous (lay eggs which hatch immediately)
• Live in intestinal tract or tissues
Classification – Intestinal Nematodes
Classification – Intestinal Nematodes
• Small Intestine only
• Ascaris lumbricoides (round worm)
• Necator americanus (american hook worm)
• Ancylostoma duodenale (hook worm)
• Strongyloides stercoralis
• Trichinella spiralis (trichina worm)

• Caecum and Vermiform appendix

• Enterobius vermicularis (pin worm)
• Trichuris trichiura (whip worm)
Modes of Infection of Nematodes
• Ingestion of:
• Embryonated eggs contaminating food & drinks, e.g. A. lumbricoides, E.
vermicularis & T. trichiura
• Growing embryos in an intermediate host (infected cyclops) e.g. D.
medinensis
• Encysted embryos in infected pig’s flesh e.g. Trichinella spiralis
• Penetration of skin:
• filariform larvae bores through the skin e.g. A. duodenale, S. stercoralis, N.
americanus
• By blood sucking insects e.g. filarial worms
• Inhalation of infected dust containing embryonated eggs e.g.
A.lumbricoides, E.vermicularis
Ascaris lumbricoides (roundworm)
• Adult worms
• Male 15 to 30 cms
• Female 20 to 45 cms, oviparous
• Eggs
• 60 µ, bile stained Albuminous coat
with unsegmented ovum
• Infective form-Embryonated
eggs
• Mode of transmission Ingestion
• Site of localization-Small
intestine
Life Cycle
• Time period from ingestion of eggs
to mature egg laying adults is
approx. 8 weeks.

• Adult worms can live in the

intestines for up to 2 years.

• Infected individuals have an output

of up to 200,000 eggs a day.
Life Cycle
Life Cycle
• About two weeks after passage in the faeces the eggs contain an
infective larval or juvenile stage.
• Humans are infected when they ingest such infective eggs.
• The eggs hatch in the small intestine, the juvenile penetrates the small
intestine and enters the circulatory system, and eventually the juvenile
worm enters the lungs.
• In the lungs the juvenile worm leaves the circulatory system and enters
the air passages of the lungs.
• The juvenile worm then migrates up the air passages into the pharynx
where it is swallowed, and once in the small intestine the juvenile
grows into an adult worm.
Life Cycle
Life Cycle

• Large mass of Ascaris

lumbricoides that was passed
from the intestinal tract.
Pathogenicity and Clinical Features

• Ascariasis – infection of A. lumbricoides

• Majority of infections are asymptomatic

• Clinical disease is largely restricted to individuals with a high worm

load

• Symptoms divided into two groups: those produced by

• Migrating larva
• Adult worms
Symptoms and Complications

• Symptoms produced by Migrating larvae

• In lungs causes the blood vessels of the lungs to haemorrhage, and there is an
inflammatory response accompanied by edema

• The resulting accumulation of fluids in the lungs results in "ascaris pneumonia

• Pneumonia (loeffler’s syndrome): fever, cough, dyspnoea, blood tinged

sputum that may contain larva, urticarial rash and eosinophilia

• Visceral larva migrans: if larvae enter systemic circulation (from pulmonary

capillaries) to reach other organs like brain, spinal cord, heart, kidney.
Symptoms and Complications
• Symptoms produced by Adult worms
• Abdominal discomfort, anorexia, nausea and diarrhoea.
• Vit. A deficiency (night blindness)
• Intestinal obstruction (particularly in children 1-5 years), intussusception
and volvulus
• Penetration through intestinal ulcer (perforation) – peritonitis
• Hypersensitivity reactions to worm Ags (toxic body fluids) – urticaria,
edema of face, conjunctivitis, irritation of URT
Pathogenicity and Clinical features
• Symptoms produced by Adult worms
• Ectopic Ascariasis – due to migration of worm up into the stomach.
• It may be:
• Vomited out
• Pass up through the oesophagus at night and comes out through mouth or nose
• Enter larynx to cause asphyxia.
• Some simply penetrate intestine, peritonitis often fatal.
• May wander down to appendix, exit anus, upwards to stomach- irritate host- vomit adult
• Migrate to other organs and cause appendicitis, cholecystitis, biliary colic, cholangitis,
pancreatitis
Laboratory Diagnosis

• Macroscopic - Direct detection of worm/s in stool or vomit

• Microscopic – direct examination of faeces following floatation

method: bile stained eggs. (eggs may not be seen at least 40 days after
infection)

• Blood examination – eosinophilia.

Treatment

• Mebendazole/ Albendazole – drug of choice but contraindicated in

pregnancy and heavy infection

• Pyrantel pamoate – single dose

• Piperazine citrate - suspected intestinal or biliary obstruction since this

drug paralyzes worms to aid expulsion.

• Levamisole
Prevention

• Good sanitation and personal hygiene

• Mass treatments with single dose mebendazole or albendazole for all

school-age children every three to four months - serves dual function:
• Treats the children and

• Reduces the overall worm burden in the community

Ancylostoma duodenale (hook worm)

• Adult worms: Male 8 -11mm Female 10-13 mm, oviparous

• Eggs: 60 µ, non bile stained (colourless) Segmented, 4 blastomeres

• Infective form: 3rd stage filariform larva

• Mode of infection: Penetration into skin

• Site of localization: Small intestine

Hookworm (Ancylostomiasis)
• Causative agent:
• Ancylostoma duodenale and
Necator americanus
• Prevalence:
• 750 million people infected
worldwide (most commonly with
Ancylostoma duodenale).
Sites of Skin Penetration

• Most common sites are:

• Thin skin between toes

• Dorsum of the feet

• Inner side of the soles

• Gardeners and miners – skin of hands

Life cycle of hookworm
Pathogenicity and Clinical Features

• Ancylostomiasis or hookworm disease, characterised by iron

deficiency anaemia

• Majority of infections are asymptomatic

• Symptoms develop in heavy infections and divided into two groups:

those produced by
• Migrating larvae

• Adult worms
Symptoms Produced by Larvae

• Lesions in the skin:

• Ancylostome dermatitis or Ground itch – occurs at the site of entry (more
common in necator), lasts for 2 to 4 weeks

• Creeping eruption – reddish itchy papule along the path traversed by filariform
larvae (larva migrans )

• Lesions in the lungs – bronchitis & bronchopneumonia.

Symptoms Produced by Adult Worm

• Epigastric pain, diarrhoea and vomiting during early phase of

infection.

• Microcytic hypochromic (Iron deficiency) anaemia – due to chronic

blood loss:
• a single adult hookworm sucks 0.2ml of blood/ day

• Haemorrhages from punctured sites

Clinical Features of Hookworm Anaemia
• Extreme pallor
• Abnormal appetite showing Pica or Geophagy – perverted taste for
earth, mud or lime
• Epigastric tenderness with dyspepsia
• Constipation
• Puffy face with swelling of lower eyelids
• Pedal oedema
• Growth retardation
• General appearance – pale plumpy with protuberant abdomen and dry
lustreless hair.
Laboratory Diagnosis

• Stool examination – microscopy: non bile stained egg, segmented

• Occult blood in stool – positive

• Blood examination – anaemia, eosinophilia

Treatment

• Mebendazole / Albendazole

• Pyrantel pamoate

• Oral iron replacement – ferrous sulphate 400mg tid

• Nutritional support

• * If Hb is below 30%, then anaemia should be treated first with Iron

till Hb comes over 50%.
Prevention and Control

• Proper sanitation measures and sewage disposal

• Personal hygiene

• Personal protection – wearing boots and gloves

• Simultaneous treatment of carriers and diseased with wholesale

treatment of community
Strongyloides stercoralis

• Adult worms: 2 - 2.5mm, ovoviviparous, eggs laid in the tissues

• Free living worms: Moist soil

• Infective form: Filariform larvae

• Mode of transmission: Penetration / autoinfection

• Site of localization: Wall of Small intestine, mainly duodenum and

jejunum Moist soil
Epidemiology

• Over 50 million people are infected worldwide

• It endemic in Africa, parts of Asia, South America, Mexico, and the

Southern US

• National survey of 216,275 stool samples in 1987 found the

prevalence of S. stercoralis to be 0.4%
Life cycle – S. stercoralis

• Penetration of intact skin by filiariform larvae in the soil, or ingestion

through contaminated food or water

• Larvae enter the circulation

• Lungs → alveoli → ascension up tracheobronchial tree → swallowed → molt
in the small bowel and mature into adult female

• Females enter the intestinal mucosa and produce several eggs daily
through parthenogenesis (hatch during transit through the gut)
Life cycle – S. stercoralis
Pathogenicity
• Skin lesions (2 types) – “larva currens”
• At the site of entry – urticarial rash
• In the perianal region – linear, erythematous urticarial wheal
• Pulmonary lesions – due to migrating larva
• Alveolar hemorrhages
• Bronchopneumonia
• Intestinal lesions - “burrowing lesions”
• Epigastric pain
• Diarrhoea with blood & mucus
• Nausea
• Weight loss
Important Terms
• Autoinfection – filariform larva
• In the Intestinal lumen
• Perineal and perianal skin penetration

• Hyperinfection – can result in autoinfection

• Steroids or Immunosuppressive therapy
• Malignancy
• Malnutrition
• Pregnancy
• Puerperium
• AIDS

• Persistence of infection – due to autoinfection

Laboratory Diagnosis

• Stool examination – rhabditiform larva

• Culture – larva

• ELISA – to detect Abs

Treatment and Prevention

• Potentially life threatening disease – treat even if its asymptomatic

• Thiabendazole for 2 days Disseminated strongyloidosis – 5 to 7 days.

Trichinella spiralis (Trichina Worm)

• Adult worms (smallest nematode infecting man): Male 1.4 – 1.6 mm

Female 3 - 4 mm, viviparous

• Infective form: Encysted larvae (100µ) in striated muscles of pig

• Mode of transmission: Ingestion of improperly cooked pork

• Site of localization: Small intestine

• Commonly involved muscles: Diaphragm, Intercostals, Deltoid

• Muscle: Pectoralis major, Biceps

Epidemiology
• Trichinella is probably best known as a parasite that humans contract from
eating raw or undercooked pork.

• Through meat inspection programs, the incidence of trichinosis in pigs has

been lowered to less than 1%, so it is unlikely (but not impossible) that pork
products purchased in your local supermarket will contain Trichinella
larvae.

• Most recent outbreaks of trichinosis in the North America have been traced
to pork products from pigs that have not been inspected and that have been
slaughtered privately.
Life Cycle – T. spiralis

• The disease in humans is zoonotic and is usually a dead end for the
parasite.

• Infected by eating raw or poorly cooked meat containing infective L1

stage larvae encysted in the muscle fibres.

• Stomach-small intestine- the worm is released from the cyst- rapidly

penetrates the mucosa where it undergoes successive moults to
become young adults, within 30 hrs post-infection.
Life Cycle – T. spiralis

• The female worms produce about 1500 larvae over about 4-6 weeks.

• Males die soon after copulation and the females die shortly after
larviposition.

• Juveniles enter the lymphatics and mesenteric veins and are found
throughout the arterial circulation between the 7th and 25th day after
infection.
Life Cycle – T. spiralis

• They travel in the circulatory system through the liver, then to the
heart, lungs.

• In striated muscles they penetrate individual muscle cells and cysts

are formed.

• Within cysts, juveniles remain viable for many years, up to 25 years in

man and 11 years in pigs.
Life Cycle – T. spiralis
Pathogenicity
• Trichinelliasis / Trichinosis – clinical features depends on the stage:
• Stage of intestinal invasion: 5-7 days, pain in abdomen, nausea, vomiting,
diarrhoea

• Stage of larval migration: fever, urticarial rash, splinter haemorrhages,

periorbital and facial oedema, damages chewing and swallowing ;
myocarditis

• 10-20%: CNS involvement

Pathogenicity

• High eosinophilia: 20-90%

• Stage of encystation: asymptomatic in light infections; myalgia,

weakness in heavy infections

• Complications – during migration:

• myocarditis, encephalitis
Pathogenicity
Laboratory Diagnosis

• Muscle biopsy – encysted larva

• Blood – eosinophilia between 2nd & 4th week

• Serology – to detect specific Abs by:

• Bentonite flocculation test

• Latex agglutination test

Treatment and Prevention

• Treatment • Prevention

• Thiabendazole and Mebendazole • Proper cooking of pork or proper

– adult worms storage

• Corticosteroids – complications • Avoidance of feeding bits and

refuse from slaughter houses and
farms to pigs – breaks life cycle.
Enterobius vermicularis (Pin Worm, Seat worm)

• Adult worms: Male 2 - 5 mm Female 8 -13 mm, oviparous

• Eggs: 60 µ, persimmon seed-like, colorless and transparent, thick and

asymmetric shell, content is a larva.

• Infective form: Embryonated egg

• Mode of transmission: Ingestion, Autoinfection

• Site of localization Large intestine – caecum and appendix

Epidemiology

• Geographical distribution—cosmopolitan in temperate zones with

about 30 to 50% of the population infected.

• It is more common in white than coloured people and more prevalent

in children than adults.

• Enterobiasis is most common where people live under crowded

conditions such as orphanages, kindergartens, and large families.
Life cycle – E. vermicularis
• The pinworms are one of the most common intestinal nematodes.

• The adult worms inhabit the caecum and colon.

• Right after mating, the male dies.

• Therefore, the male worms are rarely seen.

• The female worms migrate out the anus depositing eggs on the
perianal skin.

• Humans get this infection by mouth and by autoinfection.

Life cycle – E. vermicularis
Clinical Features
• About one-third of pinworm-
infected persons are asymptomatic
• Major symptom is anal pruritus
which associates with the nocturnal
migration of the gravid females
from the anus and deposition of
eggs in the perianal folds of the
skin.
• Restlessness, nervousness, and
irritability, probably resulting from
poor sleep associated with anal
pruritus.
• In young girls, migration of the
worms may produce vaginitis and
salpingitis or granuloma of the
peritoneal cavity.
Laboratory Diagnosis and Treatment

• Detection of adult worms in –

• Faeces

• Perianal region

• NIH swab – scrapings from perianal region

• Microscopy – non bile stained eggs

• Mebendazole, pyrantel pamoate

Treatment and Prevention
• Since the life span of the pinworm is less than two months, the major
problem is reinfection.
• Albendazole is the drug of choice. Repeated retreatment may be necessary
for a radical cure.
• Prevention:
• Treat the patients and carriers
• Individual health
• Public health
• Health education and hygienic habits
Trichuris trichiura (whipworm)
• 800 million people infected worldwide.
Life Cycle
• Fertilized infective T. trichuria eggs from contaminated soil are ingested.
• Once in the small intestine the eggs hatch and develop into a mature adult worm.
• The unembryonated eggs are passed with the stool .
• In the soil, the eggs develop into a 2-cell stage , an advanced cleavage stage , and then
they embryonate ; eggs become infective in 15 to 30 days.
• After ingestion (soil-contaminated hands or food), the eggs hatch in the small intestine,
and release larvae that mature and establish themselves as adults in the colon .
• The adult worms (approximately 4 cm in length) live in the caecum and ascending colon.
• The adult worms are fixed in that location, with the anterior portions threaded into the
mucosa.
• The females begin to oviposit 60 to 70 days after infection. Female worms in the caecum
shed between 3,000 and 20,000 eggs per day. The life span of the adults is about 1 year.
Life Cycle
Incubation and Symptoms
• Incubation Period:
• Eggs must live in the soil for 15-30 days
before becoming infective
• Once ingested it takes 2-3 days for
larvae to develop into adults
• Symptoms:
• Light infestations are generally
asymptomatic
• Abdominal pain
• Diarrhea
• Rectal prolapse
• Anemia leading to growth retardation and
cognitive impairment
Diagnosis

• Microscopic identification of Trichuria eggs or worms in faeces

• Observation during sigmoidoscopy, proctoscopy, or colonoscopy of

Trichuria worms characterized by a threadlike form with an
attenuated, whip-like end

• Identification of worms on prolapsed rectal mucosa

Treatment

• Anthelminthic such as albendazole and mebendazole, are the drugs of

choice

• Infections are generally treated for 1-3 days

• Iron supplementation in individuals with anaemia